Preeclampsia complicates up to 8% of pregnancies and accounts for significant perinatal morbidity and mortality (1, 2). No definitive etiology or specific predictors of the disease has been identified to date. Furthermore, there has been little progress in the treatment of this disorder, as the cure remains delivery of the fetus and removal of the placenta.
As early as 1915, Williams hypothesized the presence of toxic factors in the blood of women with the clinical syndrome of “toxemia” or preeclampsia (25). A number of subsequent studies, aimed at determining whether blood from pregnant women or placental extracts contained factors responsible for hypertension, yielded contradictory results (26-28). Tatum and Mule reported that whole blood collected from patients with severe preeclampsia could induce transient hypertension when transfused to the same patient in the post partum period (28). Pirani and Macgillivray reported similar observations after injecting plasma from eclamptic women 6 days after delivery (29). Since the increase in blood pressure could not be elicited by re-transfusion 6 weeks postpartum, the authors concluded that patients with preeclampsia had increased sensitivity to pressor agent(s) lasting about 1 week after delivery, but not as long as 6 weeks. Thereafter, considerable effort was devoted to the identification of the pressor agent responsible for this effect in the maternal circulation. Over the years, the focus has encompassed the renin-angiotensin system (30, 31), norepinephrine (32, 33), vasopressin (34), prostaglandins (35), endothelin (36) and others (37, 38). Despite all efforts, the factor(s) responsible for these effects remains to be elucidated.
It would be useful to be able to identify patients at risk of developing preeclampsia.